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. 2016 Feb 15;27(4):617–626. doi: 10.1091/mbc.E15-10-0703

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© 2016 Xiao et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 2: — Elevation of mucosal SPRY4-IT1 by infection with a SPRY4-IT1 lentiviral expression vector protects gut TJ barrier function in mice exposed to CLP. (A) Distribution of the lenti-SPRY4-IT1 (GFP) in the small intestinal mucosa 7 d after intraperitoneal (i.p.) injection. (B) Levels of SPRY4-IT1 in the small intestinal mucosa in mice described in A. Values are means ± SEM (n = 4). *p < 0.05 compared with C-control lentiviral vector (C-lentiviral). (C) Distribution of SPRY4-IT1 in the small intestine as measured by FISH in mice described in A. (D) Gut permeability in sham mice and mice exposed to CLP for 24 h. FITC-dextran was given orally, and blood samples were collected 4 h later. *^,+p < 0.05 compared with sham or C-lentiviral-treated mice exposed to CLP, respectively. (E) Representative immunoblots of tight junctions in the small intestinal mucosa in mice described in D. (F) Hematoxylin/eosin staining of the intestinal mucosa.